Interleukin 13 (IL‐13) alters hypoxia‐associated genes and upregulates CD73


Journal article


S. Khalil, Isaac A. Bernstein, H. Kulaga, N. Gour, N. Rowan, S. Lajoie, A. Lane
International Forum of Allergy and Rhinology, 2020

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APA   Click to copy
Khalil, S., Bernstein, I. A., Kulaga, H., Gour, N., Rowan, N., Lajoie, S., & Lane, A. (2020). Interleukin 13 (IL‐13) alters hypoxia‐associated genes and upregulates CD73. International Forum of Allergy and Rhinology.


Chicago/Turabian   Click to copy
Khalil, S., Isaac A. Bernstein, H. Kulaga, N. Gour, N. Rowan, S. Lajoie, and A. Lane. “Interleukin 13 (IL‐13) Alters Hypoxia‐Associated Genes and Upregulates CD73.” International Forum of Allergy and Rhinology (2020).


MLA   Click to copy
Khalil, S., et al. “Interleukin 13 (IL‐13) Alters Hypoxia‐Associated Genes and Upregulates CD73.” International Forum of Allergy and Rhinology, 2020.


BibTeX   Click to copy

@article{s2020a,
  title = {Interleukin 13 (IL‐13) alters hypoxia‐associated genes and upregulates CD73},
  year = {2020},
  journal = {International Forum of Allergy and Rhinology},
  author = {Khalil, S. and Bernstein, Isaac A. and Kulaga, H. and Gour, N. and Rowan, N. and Lajoie, S. and Lane, A.}
}

Abstract

Interleukin 13 (IL‐13) is a pleiotropic cytokine that has been shown to be important in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP) and other type 2 inflammation–related diseases. Increased IL‐13 expression can elicit several pro‐inflammatory effects, including eosinophilia, and pathology such as increased mucus secretion. Polypogenesis in chronic rhinosinusitis (CRS) can be caused by hypoxia, which can also lead to hyperpermeability of airway epithelium and epithelium‐to‐mesenchymal translation through the upregulation of hypoxia‐associated genes, such as HIF1. Whether T‐helper 2 (Th2) inflammatory cytokines, such as IL‐13, can also induce sinonasal epithelial hypoxia‐associated genes is currently unknown.


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